A study was conducted to compare the toxicity and bioavailability of lead from diverse environmental sources could vary, depending on the source (dust, lead ore, mine tailings, spills, etc.). The hazardous risk to humans and thus need for removal of the source of lead material must be determined. An animal model using F344 rats was developed to compare the toxicity and bioavailability of pure lead salts with relevant environmental sources of lead contamination. Studies with lead ore from Skagway AK, indicated lead could be absorbed, accumulate in vital organs, and with longer exposure, might result in toxic responses. Sources of lead from other mining sites in Alaska, Missouri, and Colorado were investigated in more lengthy studies to determine if greater toxicity would ensue. Lead ore samples from Alaska, Missouri, and Colorado mines were fed to rats for 90 days to compare the materials from different areas. Male F344 rats were fed lead acetate, oxide, sulfide, and lead ore concentrate from Skagway, AK, for 30 days to compare the toxicity and bioavailability of these materials. The soluble lead acetate and oxide accumulated to a greater degree in bone and soft tissues than the less soluble lead sulfide and lead ore, but there was a strong correlation between dose and bone lead irrespective of source. The aminolevulinic acid biomarker was ineffective below 20 microg/g bone lead. Blood lead was about 80 microg/g in rats fed soluble leads, and about 20 microg/g in those fed less soluble leads. Rats fed soluble leads accumulated about 10-fold higher kidney and brain lead than those fed less soluble leads. However, detectable and potentially toxic lead concentrations accumulated in kidney and brain of rats fed lead ore or lead sulfide, suggesting that with longer exposure more lead would accumulate. Kidney lesions occurred in rats dosed with 30 or 100 ppm lead acetate but not in other treatment groups.